Longitudinal Changes in Epigenetic Age Acceleration in Aviremic Human Immunodeficiency Virus–Infected Recipients of Long-term Antiretroviral Treatment. (24th June 2021)

• Record Type: Journal Article
• Authors: Esteban-Cantos, Andrés; Montejano, Rocio; Rodríguez-Centeno, Javier; Saiz-Medrano, Gabriel; De Miguel, Rosa; Barruz, Pilar; Bernardino, Jose I; Mena-Garay, Beatriz; Cadiñanos, Julen; Jiménez-González, María; Nevado, Julián; Valencia, Eulalia; Mayoral-Muñoz, Mario; Arribas, Jose R; Rodés, Berta
• Is Part Of: Journal of infectious diseases. Volume 225:Number 2(2022)
• Page Start: 287
• Page End: 294
• Publication Date: 2021-06-24
• Subjects: HIV infection -- antiretroviral therapy -- aging -- epigenetic age acceleration; Communicable diseases -- Periodicals; Diseases -- Causes and theories of causation -- Periodicals; Medicine -- Periodicals; Communicable Diseases -- Periodicals; Electronic journals; 616.9
• DOI: 10.1093/infdis/jiab338
• Languages: English
• ISSNs: 0022-1899

Abstract

Abstract : Epigenetic aging, according to 3 different epigenetic clocks, did not accelerate in a cohort of long-term aviremic HIV-infected adults after 4 years of follow-up. Measures of epigenetic age acceleration might be useful tools to predict the occurrence of clinical outcomes. Abstract: Background: Human immunodeficiency virus (HIV) infection induces epigenetic age acceleration (EAA), but it remains unclear whether epigenetic aging continues to accelerate during successful antiretroviral therapy (ART) and prolonged virological suppression. Methods: We longitudinally analyzed 63 long-term aviremic HIV-infected adults. Using blood DNA methylation patterns, we calculated EAA measures based on 3 epigenetic clocks (Horvath's clock, PhenoAge, and GrimAge). We recorded the emergence of serious AIDS-related and non-AIDS-related events throughout the study to assess its association with EAA. Results: All participants were on stable ART and were virologically suppressed. After 4 years of follow-up, PhenoAge-EAA and GrimAge-EAA showed no differences, whereas Horvath-EAA slightly decreased (median difference, –0.53 years; P = .015). Longitudinal changes in EAA measures were independent of changes in CD4 cell counts, the ART regimen, or other HIV-related factors. Nineteen percent of participants experienced a serious clinical event during the study. Horvath-EAA was significantly higher at baseline in participants with clinical events ( P = .027). After adjusting for confounders, we found a trend toward an association of higher levels of all EAA measures at baseline with serious clinical events. Conclusions: Epigenetic aging did not accelerate in long-term aviremic HIV-infected adults after 4 years of successful ART. EAA measures deserve further study as potential tools for predicting clinical events.